Cardiac glycosides have been recognized as potential cancer drugs at least since 1999 (Haux, Med. Hypotheses. 53:543-8, 1999) and extensive studies of their cytotoxicity in human cancer cells were carried out as early as 2001 (Johansson, et al., Anticancer Drugs. 12:475-83, 2001). Interest in the mechanism of inhibition of the cardiac glycosides' target, the inotropic Na,K-ATPases found in the membranes of animal cells, has spawned a considerable body of work (Mijatovic, et al., Biochim Biophys Acta. 1776:32-57, 2007). Extensive medicinal chemistry research directed at finding more potent and less toxic cardiac glycosides through chemical modification of their steroid and sugar portions has also been conducted (Repke, K. R., et al., Progress in Medicinal Chemistry. 30:135-202, 1993; Mudge, et al., Circ Res. 43:847-54, 1978; Repke, K. R. H., Drug Discovery Today. 2:110-16, 1997). Yet despite the synthesis of many different analogs (Repke, K. R., et al., Progress in Medicinal Chemistry. 30:135-202, 1993; Schneider and Wolfling, Curr Org Chem. 8:1381-403, 2004), some of which include the synthesis of specific cardiac glycosides as cancer drugs, exemplified by the work on digitoxin neoglycoside analogs (Langenhan, et al., Proc Natl Acad Sci USA. 102:12305-10, 2005) and on proscillaridin analogs (Gardiner, et al., USPTO. A1:1-67, 2009), few cardiac glycosides are currently undergoing clinical development—perhaps due to the widespread belief that cardiac glycosides cannot be used for cancer therapeutically without significant toxicity to heart and neural tissues.